Experimental Stroke Drug Protects Brain

Synthetic LAU-0901 molecule may safeguard brain after stroke

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) Researchers have long searched for additional methods for protecting the brain from potential damage following a stroke. An experimental stroke drug may lessen the severity of damage.

A synthetic low-weight molecule capable of crossing the blood-brain barrier called LAU-0901 has been shown to protect the brain during an early experimental stroke model study.

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Dr. Nicolas Bazan, Boyd Professor and director of the Neuroscience Center of Excellence at Louisiana State University Health Sciences Center New Orleans and lead study researcher, already has been issued a patent for the molecule that he said could play an important role in preserving brain function after a stroke.

When an ischemic stroke occurs, the body releases signals that cause neuroinflammation. This may lead to a buildup of harmful chemicals in the brain. Inhibiting this process of accumulating platelet-activating factor could help neurons survive, protecting the brain from damage.

Dr. Bazan said that  LAU-0901 can successfully lessen incorrect signaling and inhibit the platelet-activating factor, which was shown to greatly lessen the severity of damage in an experimental stroke.

MRI imaging and microscopic tissue studies were also used to examine the impact of the molecule. Investigators found that LAU-0901 successfully lessened the severity of brain damage in an experimental stroke model when given within two hours of the onset of stroke symptoms. The experimental drug also was shown to reduce brain lesions and improve coordination and movement.

No side effects have been noted. Researchers expect the molecule could form the basis for new therapies to protect the brain function of ischemic stroke patients.

While thrombolytic tissue plasminogen activator (tPA), is currently available to treat stroke patients, only about 5 percent of ischemic stroke patients are eligible for the treatment which must be given within 4.5 hours of the onset of stroke symptoms.

The research, which was supported by grants from the National Institute of Neurological Disorders and Stroke and the National Institute on Aging of the National Institutes of Health, was published in the March issue of Translational Stroke Research.

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Review Date: 
February 29, 2012
Last Updated:
March 1, 2012